scholarly journals Predicting signaling pathways regulating demyelination in a rat model of lithium-pilocarpine-induced acute epilepsy: A proteomics study

2021 ◽  
Author(s):  
Peng Wang ◽  
Kang Ma ◽  
Lu Yang ◽  
Guodong Zhang ◽  
Mengyi Ye ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Rat Model ◽  
Proteomics Study

Repetitive restriction of muscle blood flow enhances mTOR signaling pathways in a rat model

2016 ◽  
Vol 31 (10) ◽  
pp. 1685-1695 ◽  
Author(s):  
Toshiaki Nakajima ◽  
Tomohiro Yasuda ◽  
Seiichiro Koide ◽  
Tatsuya Yamasoba ◽  
Syotaro Obi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Signaling Pathways ◽  
Rat Model ◽  
Muscle Blood Flow ◽  
Mtor Signaling

scholarly journals Qiliqiangxin Attenuates Cardiac Remodeling via Inhibition of TGF-β1/Smad3 and NF-κB Signaling Pathways in a Rat Model of Myocardial Infarction

2018 ◽  
Vol 45 (5) ◽  
pp. 1797-1806 ◽  
Author(s):  
Anbang Han ◽  
Yingdong Lu ◽  
Qi Zheng ◽  
Jian Zhang ◽  
YiZhou Zhao ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Cardiac Function ◽  
Signaling Pathways ◽  
Rat Model ◽  
Cardiac Remodeling ◽  
Left Ventricular ◽  
Protective Effects ◽  
Tnf Α ◽  
Tgf Β1

Background/Aims: Qiliqiangxin (QL), a traditional Chinese medicine, has been demonstrated to be effective and safe for the treatment of chronic heart failure. Left ventricular (LV) remodeling causes depressed cardiac performance and is an independent determinant of morbidity and mortality after myocardial infarction (MI). Our previous studies have shown that QL exhibits cardiac protective effects against heart failure after MI. The objective of this study was to explore the effects of QL on myocardial fibrosis in rats with MI and to investigate the underlying mechanism of these effects. Methods: A rat model of acute myocardial infarction was induced by ligating the left anterior descending coronary artery. The rats were treated with QL (1.0 g/kg/day) for 4 weeks after surgery. Echocardiography and histology examination were performed to evaluate heart function and fibrosis, respectively. Protein levels of transforming growth factor-β1 (TGF-β1), phosphorylated Smad3 (p-Smad3), phosphorylated Smad7 (p-Smad7), collagen I (Col- I), alpha smooth muscle actin (a-SMA), tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), nuclear factor κB (NF-κB), and phosphorylated inhibitor of kappa B alpha (p-IκBα) were measured by western blot analysis. Results: QL treatment ameliorated adverse cardiac remodeling 8 weeks after AMI, including better preservation of cardiac function, decreased inflammation, and reduced fibrosis. In addition, QL treatment reduced Col-I, a-SMA, TGF-β1, and p-Smad3 expression levels but increased p-Smad7 levels in postmyocardial infarct rat hearts. QL administration also reduced the elevated levels of cardiac inflammation mediators, such as TNF-α and IL-6, as well as NF-κB and p-IκBα expression. Conclusions: QL therapy exerted protective effects against cardiac remodeling potentially by inhibiting TGF-β1/Smad3 and NF-κB signaling pathways, thereby preserving cardiac function, as well as reducing myocardial inflammation and fibrosis.

scholarly journals Quantitative proteomics reveals the effect of Yigu decoction (YGD) on protein expression in bone tissue

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Ruikun Zhang ◽  
Kun Yan ◽  
Yulun Wu ◽  
Xinmiao Yao ◽  
Guijin Li ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Bone Tissue ◽  
Rat Model ◽  
Quantitative Proteomics ◽  
Protective Mechanism ◽  
Mineral Density ◽  
Biologically Relevant ◽  
Increased Risk ◽  
Specific Pathogen ◽  
The Right

Abstract Background Osteoporosis (OP) is a systemic bone disease characterized by decreased bone mass, destruction of the bone tissue microstructure, increased bone brittleness and an increased risk of fracture. OP has a high incidence rate and long disease course and is associated with serious complications. Yigu decoction (YGD) is a compound prescription in traditional Chinese medicine that is used to treat OP. However, its mechanism in OP is not clear. This study used a tandem mass tag (TMT)quantitative proteomics method to explore the potential bone-protective mechanism of YGD in an osteoporotic rat model. Materials and methods A rat model of OP was established by ovariectomy. Eighteen 12-week-old specific-pathogen-free female Wistar rats weighing 220 ± 10 g were selected. The eighteen rats were randomly divided into 3 groups (n = 6 in each group): the normal, model and YGD groups. The right femurs from each group were subjected to quantitative biological analysis. TMT quantitative proteomics was used to analyze the proteins extracted from the bone tissue of rats in the model and YGD groups, and the differentially expressed proteins after intervention with YGD were identified as biologically relevant proteins of interest. Functional annotation correlation analysis was also performed to explore the biological function and mechanism of YGD. Result Compared with the model group, the YGD group showed significant upregulation of 26 proteins (FC > 1.2, P < 0.05) and significant downregulation of 39 proteins (FC < 0.833, P < 0.05). Four important targets involved in OP and 5 important signaling pathways involved in bone metabolism were identified. Conclusions YGD can significantly increase the bone mineral density (BMD) of osteoporotic rats and may play a therapeutic role by regulating target proteins involved in multiple signaling pathways. Therefore, these results improve the understanding of the OP mechanism and provide an experimental basis for the clinical application of YGD in OP treatment.

scholarly journals Proteins and Signaling Pathways Response to Dry Needling Combined with Static Stretching Treatment for Chronic Myofascial Pain in a RAT Model: An Explorative Proteomic Study

2019 ◽  
Vol 20 (3) ◽  
pp. 564 ◽  
Author(s):  
Lihui Li ◽  
Qiangmin Huang ◽  
Marco Barbero ◽  
Lin Liu ◽  
Thitham Nguyen ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Rat Model ◽  
Large Scale ◽  
Myofascial Pain ◽  
Dominant Role ◽  
Mass Spectrometry Analysis ◽  
Static Stretching ◽  
Dry Needling ◽  
Myofascial Trigger Points ◽  
Network Analyses

A quantitative proteomic analysis of the response to dry needling combined with static stretching treatment was performed in a rat model of active myofascial trigger points (MTrPs). 36 rats were divided into a model group (MG), a stretching group (SG) and a dry needling combined with stretching group (SDG). We performed three biological replicates to compare large-scale differential protein expression between groups by tandem mass tag (TMT) labeling technology based on nanoscale liquid chromatography mass spectrometry analysis (LC–MS/MS). Hierarchical clustering, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment and protein-protein interaction network analyses were performed for the general characterization of overall enriched proteins. For validation of the results of TMT, the candidate proteins were verified by parallel reaction monitoring (PRM) analysis. 285 differentially expressed proteins between groups were identified and quantified. Tight junction pathway played a dominant role in dry needling combined with static stretching treatment for the rat model of active MTrPs. Three candidate proteins, namely actinin alpha 3, calsequestrin-1 and parvalbumin alpha, were further validated, consistent with the results of LC–MS/MS. This is the first proteomics-based study to report the therapeutic mechanism underlying dry needling and static stretching treatment for MTrPs. Further functional verification of the potential signaling pathways and the enriched proteins is warranted.

Radiosurgery inhibition of the Notch signaling pathway in a rat model of arteriovenous malformations

2014 ◽  
Vol 120 (6) ◽  
pp. 1385-1396 ◽  
Author(s):  
Jian Tu ◽  
Yang Li ◽  
Zhiqiang Hu ◽  
Zhongbin Chen
Keyword(s):  
Endothelial Cells ◽  
Notch Signaling ◽  
Signaling Pathways ◽  
Rat Model ◽  
Arteriovenous Malformations ◽  
Proximity Ligation Assay ◽  
Gene Target ◽  
Thrombotic Occlusion ◽  
Time Points ◽  
Notch1 Receptor

Object Notch signaling has been suggested to promote the development and maintenance of arteriovenous malformations (AVMs), but whether radiosurgery inhibits Notch signaling pathways in AVMs is unknown. The aim of this study was to examine molecular changes of Notch signaling pathways following radiosurgery and to explore mechanisms of radiosurgical obliteration of “nidus” vessels in a rat model of AVMs. Methods One hundred eleven rats received common carotid artery–to–external jugular vein anastomosis to form an arteriovenous fistula (AVF) model. Six weeks postoperatively, dilated small vessels and capillaries formed a nidus. The rats with AVFs received 25-Gy radiosurgery. The expression of Notch1 and Notch4 receptors and their ligands, Delta-like1 and Delta-like4, Jagged1, Notch downstream gene target HES1, and an apoptotic marker caspase-3 in nidus vessels in the AVF rats was examined immunohistochemically and was quantified using LAS-AF software at 7 time points over a period of 42 days postradiosurgery. The interaction events between Notch1 receptor and Jagged1, as well as Notch4 receptor and Jagged1, were quantified in nidus vessels in the AVF rats using proximity ligation assay at different time points over 42 days postradiosurgery. Results The expression of Notch1 and Notch4 receptors, Delta-like1, Delta-like4, Jagged1, and HES1 was observed in nidus vessels in the AVF rats pre- and postradiosurgery. Radiosurgery enhanced apoptotic activity (p < 0.05) and inhibited the expression of Notch1 and Notch4 receptors and Jagged1 in the endothelial cells of nidus vessels in the AVF rats at 1, 2, 3, 7, 21, 28, and 42 days postradiosurgery (p < 0.05). Radiosurgery suppressed the interaction events between Notch1 receptor and Jagged1 (p < 0.001) as well as Notch4 receptor and Jagged1 (p < 0.001) in the endothelial cells of nidus vessels in the AVF rats over a period of 42 days postradiosurgery. Radiosurgery induced thrombotic occlusion of nidus vessels in the AVF rats. There was a positive correlation between the percentage of fully obliterated nidus vessels and time after radiosurgery (r = 0.9324, p < 0.001). Conclusions Radiosurgery inhibits endothelial Notch1 and Notch4 signaling pathways in nidus vessels while inducing thrombotic occlusion of nidus vessels in a rat model of AVMs. The underlying mechanisms of radiosurgery-induced AVM shrinkage could be a combination of suppressing Notch receptor signaling in blood vessel endothelial cells, leading to a reduction in nidus vessel size and thrombotic occlusion of nidus vessels.

scholarly journals Formaldehyde up-regulates TRPV1 through MAPK and PI3K signaling pathways in a rat model of bone cancer pain

2012 ◽  
Vol 28 (2) ◽  
pp. 165-172 ◽  
Author(s):  
Ying Han ◽  
Yan Li ◽  
Xing Xiao ◽  
Jia Liu ◽  
Xiang-Ling Meng ◽  
...  
Keyword(s):  
Cancer Pain ◽  
Signaling Pathways ◽  
Rat Model ◽  
Bone Cancer ◽  
Bone Cancer Pain ◽  
Pi3k Signaling
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